It is well known that light, UVA light in particular, is damaging to skin cells. Phototoxic cell damage occurs via the reaction of light with certain compounds that are endogenous to skin. The mechanism by which the photodamage occurs is well understood, and can be described, briefly, as follows. The molecules involved, which may be referred to as sensitizers or even accelerators of skin damage, react with light and, in the presence of oxygen, result in the formation of “reactive oxygen species”, or “ROS.” It is these molecules, i.e., ROS molecules, which are involved in pathways leading to cell damage, including carcinogenesis and photoaging, but not being limited to these phenomena. More details of this phenomenon may be found in Wondrak, et al. J. Invest. Dermatol 119:489–498 (2002), the entirety of which is incorporated by reference.
The fact that molecules endogenous to, e.g., the skin, are involved in accelerated phototoxicity suggests targeted therapy. To elaborate, if a compound is essentially inert in the absence of light but is involved in cellular destruction upon contact with light, then such compounds could be used in situations where targeted cell death is desired. Such situations include, but are not limited to, psoriasis, acne, premalignant and malignant hyperproliferative disorders such as actinic keratosis, and other conditions well known to the art.
Conversely, the existence of the photoactivable molecules suggests the existence of molecules which act to quench or to inhibit the effect of light on cells. Such quenchers or inhibitors can be used in situations where the harmful effects of light need to be reversed, and/or inhibited. Such quenchers or inhibitors may be used prophylactically, as well as therapeutically.
Hence, the modulation of phototoxicity on cells is the focus of the invention described herein, as will be seen in the disclosure which follows. Modulators, as used herein, refers to molecules which may be derived from skin components, collagen in particular.